Smoking and Endothelial Progenitor Cells: A Revision of Literature

Abstract

Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) derived from bone marrow contribute to reendothelialization of injuried vessels as well as neo-vascularization of ischemic lesions in either a direct or an indirect way. Moreover, the number and/or the functional activity of EPCs are inversely correlated with risk factors for cardiovascular disease. Among the different risk factors, cigarette smoking is a major cause of reducing the numbers and function of circulating EPCs. This review is a revision of recent literature on EPC alteration associated with smoking. In particular, we show the recent observation on the effects of active and second hand smoke (SHS) exposure on EPC number and functional activity. This review also considers the effects of nicotine and other smoke compounds on EPC number and activity, in in vitro and in vivo models.

Ambient Fine Particulate Matter Induces Apoptosis of Endothelial Progenitor Cells Through Reactive Oxygen Species Formation

“…Some studies have shown that SHS, PM and other pollutants such as nickel and acrolein are able to decrease the number and function of circulating EPCs [11,29]. The potential mechanisms are believed to be related to impaired VEGF-mediated signaling that compromised the mobilization of bone marrow-derived EPCs to the circulation [30] or blocking nitric oxide production [31].…”

Difference in mobilization of progenitor cells after myocardial infarction in smoking versus non-smoking patients: insights from the BONAMI trial

“…Among them, smoking critically reduces the number and function of circulating EPCs in chronic coronary disease as well as in active smokers without coronary disease [6]. In our study, the number of either bone marrow or blood CD45dimCD34 + KDR+/10 5 WC cells were decreased in active smokers and their migratory response impaired, as compared to non/former smoking patients.…”

“…Circulating EPCs isolated from patients with coronary artery disease have previously been shown to have an impaired migratory response, which is inversely correlated with the number of cardiovascular risk factors [15]. A reduced number of EPCs may be due to a variety of mechanisms, including exhaustion of the pool of progenitor cells in the bone marrow, impaired functional capacity within the bone marrow, reduced mobilization of EPCs, or reduced survival and/or differentiation of mobilized EPCs [6,14]. The presence of ‘good and poor mobilizers’ post-AMI is well-known [16].…”

“…One hypothesis for such discrepancies is wide inter-patient variability in cell functionality. This issue is particularly relevant to the use of autologous bone marrow cells, the function of which is decreased by advanced age [3], and the risk factors for atherosclerosis [4-6] which implies that these patients are at risk of being treated with cells that are intrinsically defective. The prognostic impact of this altered pattern is reflected by the predictive value of the colony forming unit (CFU) capacity of the infused cells on the treatment outcome in chronic ischemic heart disease [7].…”

C-Kit/c-Kit ligand interaction of bone marrow endothelial progenitor cells is influenced in a cigarette smoke extract-induced emphysema model

“…Smoking influences the number of circulating EPCs in COPD, as circulating EPCs are markedly reduced in chronic smokers [9][10][11]. The proliferative ability of circulating EPCs isolated from smokers is significantly inhibited in vitro [12].…”